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1.
Am J Transl Res ; 14(1): 55-67, 2022.
Artículo en Inglés | MEDLINE | ID: mdl-35173829

RESUMEN

BACKGROUND: With a high incidence globally, deaths form gastric cancer (GC) are not rare. Early diagnosis is crucial to ameliorate its prognosis. Confocal laser endomicroscopy (CLE) and narrow band imaging (NBI) have been extensively applied in gastroscopy, particularly when it comes to the detection and management of premalignant gastric lesion. Our meta-analysis intends to appraise the diagnostic capability and compare the efficacy of NBI and CLE for focal precancerous state of gastric cancer. METHODS: We performed a literature search up to November 5, 2020 in online databases and major conferences. Two investigators assessed the methodological bias by QUADAS-2, followed by sophisticated study selection and data exaction to make a comparison between sensitivity, specificity, positive and negative likelihood values, and diagnostic odds ratio. A symmetric summary receiver-operating curve (sROC) and its area under the curve (AUC) were used to estimate threshold effect. Additionally, we evaluated the publication bias by Deeks' asymmetry test. RESULTS AND CONCLUSIONS: Four studies involved 248 patients and 526 lesions. In analysis drawn from every lesion, the NBI's pooled sensitivity and specificity were 87% (95% CI: 0.80-0.92) and 85% (95% CI: 0.75-0.91), and those of CLE were 90% (95% CI: 0.85-0.91) and 87% (95% CI: 0.83-0.91). CLE illustrated that the pooled two were slightly higher than NBI when compared at the level of every lesion. The AUC for NBI and CLE was 0.92 (0.90-0.94) and 0.95 (0.92-0.96), and there might be a threshold effect, according to the shoulder-like distribution of scatter points in the sROC. We did not find obvious publication bias in our meta-analysis.

2.
Chin J Nat Med ; 19(2): 143-152, 2021 Feb.
Artículo en Inglés | MEDLINE | ID: mdl-33641785

RESUMEN

Drug resistance is a major obstacle in the development of effective colorectal cancer (CRC) therapy. Our study aimed to explore the reversal abilities of Jiedu Sangen decoction (JSD) on the 5-fluorouracil (5-FU) resistance and its underlying molecular mechanisms. Expression changes in HIF-1 of CRC tissues were firstly revealed by bioinformatics analysis. Afterwards, cell viabilities of JSD and 5-FU treatments on 5-FU resistant human colon cancer cells (HCT-8/5-FU) were determined. Expressions of phosphoinositide 3-kinase (PI3K), protein kinase B (AKT)/p-AKT, hypoxia-inducible factor 1 (HIF-1α), as well as glycolysis related proteins such as L-lactate dehydrogenase A (LDHA), Glucose transporter type 1 (Glut1), Hexokinase 2 (HKII), and cysteinyl aspartate specific proteinase (Caspase) family members in HCT-8/5-FU cells, HIF-1α silenced HCT-8/5-FU cells and tumor tissues were detected by western blotting. HIF-1α was found over expressed in CRC tissues according to public available datasets in Oncomine. Growth inhibition rates of HCT-8/5-FU cells were increased along with the increase of JSD concentrations. JSD caused down-regulated HIF-1α, PI3K, AKT/p-AKT, HKII and Glut1, as well as up-regulated Caspase3 and Caspase9 in HCT-8/5-FU cells and tumor tissues. In HIF-1α silenced HCT-8/5-FU cells, synergistic group showed significantly reduced expression levels of PI3K, AKT, p-AKT. Additionally, up-regulated expressions of Caspase6 and Caspase7 were observed. JSD combined with 5-FU also exhibited obvious inhibitory efficiency on tumor growth in vivo. JSD may reverse 5-FU resistance by suppressing glycolysis via PI3K/AKT/HIF-1α signaling pathway, thereby inhibiting glycolysis and induce apoptosis to enhance anti-tumor activity.


Asunto(s)
Neoplasias Colorrectales , Resistencia a Antineoplásicos , Medicamentos Herbarios Chinos/farmacología , Fluorouracilo , Transducción de Señal/efectos de los fármacos , Línea Celular Tumoral , Neoplasias Colorrectales/tratamiento farmacológico , Neoplasias Colorrectales/genética , Fluorouracilo/farmacología , Glucólisis , Humanos , Subunidad alfa del Factor 1 Inducible por Hipoxia/genética , Subunidad alfa del Factor 1 Inducible por Hipoxia/metabolismo , Fosfatidilinositol 3-Quinasas/genética , Fosfatidilinositol 3-Quinasas/metabolismo , Proteínas Proto-Oncogénicas c-akt/genética , Proteínas Proto-Oncogénicas c-akt/metabolismo
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